Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during ventricular systole. Common causes include mitral valve prolapse, rheumatic fever, and functional regurgitation secondary to LV dilation or infarction. Complications include progressive heart failure, arrhythmias, and endocarditis. Symptoms and signs include palpitations, dyspnea, and a holosystolic apical murmur. Diagnosis is by physical examination and echocardiography. Prognosis depends on LV function and severity and duration of MR. Patients with mild, asymptomatic MR may be monitored, but progressive or symptomatic MR requires mitral valve repair or replacement.
MR may be acute or chronic.
Causes of acute MR include
Common causes of chronic MR include those of acute MR plus
Uncommon causes of chronic MR include a congenital endocardial cushion defect with a cleft anterior leaflet, SLE, acromegaly, myxoma involving the valve or chordae, and calcification of the mitral annulus (mainly in elderly women).
Functional regurgitation occurs through a normal valve that is distorted by LV remodeling. Causes include dilated cardiomyopathy and regional or global myocardial ischemia.
In infants, the most likely causes of MR are papillary muscle dysfunction, endocardial fibroelastosis, acute myocarditis, cleft mitral valve with or without an endocardial cushion defect, and myxomatous degeneration of the mitral valve. MR may coexist with mitral stenosis when thickened valvular leaflets do not close.
Acute MR may cause acute pulmonary edema and cardiogenic shock or sudden cardiac death. Complications of chronic MR include gradual enlargement of the left atrium (LA); LV enlargement and eccentric hypertrophy, which initially compensates for regurgitant flow (preserving forward stroke volume) but eventually decompensates (reducing forward stroke volume); atrial fibrillation (AF), which may be further complicated by thromboembolism; and infective endocarditis.
Symptoms and Signs
Acute MR causes the same symptoms and signs as acute heart failure and cardiogenic shock. Specific signs of mitral regurgitation may be absent (see Coronary Artery Disease: Hypotension and cardiogenic shock). Most patients with chronic MR are initially asymptomatic and develop symptoms insidiously as the LA enlarges, pulmonary artery and venous pressure increases, and LV compensation fails. Symptoms include dyspnea, fatigue (due to heart failure), orthopnea, and palpitations (often due to AF). Rarely, patients present with endocarditis (eg, fever, weight loss, embolic phenomena).
Signs develop only when MR becomes moderate to severe. Inspection and palpation may detect a brisk apical impulse and sustained left parasternal movement due to systolic expansion of an enlarged LA. An LV impulse that is sustained, enlarged, and displaced downward and to the left suggests LV hypertrophy and dilation. A diffuse precordial lift occurs with severe MR because the LA enlarges, causing anterior cardiac displacement, and pulmonary hypertension causes right ventricular hypertrophy. A regurgitant murmur (or thrill) may also be palpable in severe cases.
On auscultation, the 1st heart sound (S1) may be soft (or occasionally loud). A 3rd heart sound (S3) at the apex reflects a dilated LV and important MR.
The cardinal sign of MR is a holosystolic (pansystolic) murmur, heard best at the apex with the diaphragm of the stethoscope when the patient is in the left lateral decubitus position. In mild MR, the systolic murmur may be abbreviated or occur late in systole. The murmur begins with S1 in conditions causing leaflet incompetency throughout systole, but it often begins after S1 (eg, when chamber dilation during systole distorts the valve apparatus or when myocardial ischemia or fibrosis alters dynamics). When the murmur begins after S1, it always continues to the 2nd heart sound (S2). The murmur radiates toward the left axilla; intensity may remain the same or vary. If intensity varies, the murmur tends to crescendo in volume up to S2. MR murmurs increase in intensity with handgrip or squatting because peripheral vascular resistance to ventricular ejection increases, augmenting regurgitation into the LA; murmurs decrease in intensity with standing or the Valsalva maneuver. A short rumbling mid-diastolic inflow murmur due to torrential mitral diastolic flow may be heard following an S3 . In patients with posterior leaflet prolapse, the murmur may be coarse and radiate to the upper sternum, mimicking aortic stenosis.
MR murmurs may be confused with tricuspid regurgitation, which can be distinguished because its murmur is augmented during inspiration.
Diagnosis is suspected clinically and confirmed by echocardiography. Doppler echocardiography is used to detect regurgitant flow and pulmonary hypertension. Two-dimensional or 3-dimensional echocardiography is used to determine the cause and severity of MR, the presence and extent of annular calcification, and the size and function of the LV and LA and to detect pulmonary hypertension. When acute, severe MR may not be apparent on color Doppler echocardiography, but suspicion is raised when acute heart failure is accompanied by hyperdynamic LV systolic function.
If endocarditis or valvular thrombi are suspected, transesophageal echocardiography (TEE) can provide a more detailed view of the mitral valve and LA. TEE is also indicated when mitral valve repair instead of replacement is being considered to confirm the anatomy in more detail.
An ECG and chest x-ray are usually obtained initially. ECG may show LA enlargement and LV hypertrophy with or without ischemia. Sinus rhythm is usually present when MR is acute because the atria have not had time to stretch and remodel.
Chest x-ray in acute MR may show pulmonary edema; abnormalities in cardiac silhouette are not evident unless an underlying chronic disorder is also present. Chest x-ray in chronic MR may show LA and LV enlargement. It may also show pulmonary vascular congestion and pulmonary edema with heart failure.
Cardiac catheterization is done before surgery, mainly to determine whether coronary artery disease (CAD) is present. A prominent systolic c-v wave is seen on pulmonary artery occlusion pressure (pulmonary capillary wedge pressure) tracings during ventricular systole. Ventriculography can be used to quantify MR. Cardiac MRI can accurately measure regurgitant fraction and determine the cause of dilated myopathy with MR. Exercise echocardiography and serum brain natriuretic peptide (BNP) have been proposed as aids to decide the timing of surgery in asymptomatic patients, but are not used widely.
Prognosis varies by acuity and cause of MR. Once MR becomes severe, about 10% of asymptomatic patients become symptomatic per year thereafter. About 10% of patients with chronic MR caused by MVP require surgical intervention.
Acute MR requires emergency mitral valve repair or replacement with concomitant coronary revascularization as necessary. Pending surgery, nitroprusside or nitroglycerin infusion may be used to reduce afterload, thus improving forward stroke volume and reducing ventricular and regurgitant volume.
Definitive treatment of chronic MR is mitral valve repair or replacement, but patients with asymptomatic or mild chronic MR and no pulmonary hypertension or AF do well with periodic monitoring. ACE inhibitors and other vasodilators do not delay LV dilation or MR progression and so have no role in asymptomatic MR with preserved LV function. However, if LV dilation or dysfunction is present, vasodilators, spironolactone, and vasodilating β-blockers (eg, carvedilol) are indicated. If the ECG shows left bundle branch block, then biventricular pacing may be beneficial for functional MR. Loop diuretics such as furosemide are helpful in patients with exertional or nocturnal dyspnea. Digoxin may reduce symptoms in patients with AF or those in whom valve surgery is not appropriate.
Mitral valve repair or replacement improves outcomes and decreases the chance of LV function worsening (except in functional MR, for which no satisfactory intervention exists because it is caused by LV dysfunction rather than abnormalities of the mitral valve itself). Intervention is indicated at the onset of heart failure symptoms or echocardiographically defined decompensation (end-diastolic dimension > 70 mm, end-systolic dimension > 40 to 45 mm, ejection fraction < 60%, or pulmonary artery systolic pressure > 50 mm Hg). Patients who are highly likely to require repair (based on valve anatomy and clinical judgment) may undergo surgery before reaching these endpoints, especially if AF develops. Selected patients with AF benefit from concomitant ablation therapy, although this therapy increases operative morbidity.
The closer the mitral valve intervention mimics the native valve, the better for LV preservation and mortality. Hence, repair is preferred over replacement with chordal preservation, which is preferred over replacement with removal of chordae. Mechanical prostheses are preferred because tissue valves have reduced longevity in the mitral position. Mitral repair with an annuloplasty ring often provides only temporary relief of MR but is usually done at the time of coronary artery bypass grafting if the MR is moderate or greater. New percutaneous procedures that tailor the mitral leaflets have been used in elderly and high-risk patients, and percutaneous placement of artificial valves is under trial.
In about 50% of decompensated patients, prosthetic valve implantation markedly depresses ejection fraction because in such patients, ventricular function has become dependent on the afterload reduction of MR.
Antibiotic prophylaxis is no longer recommended except for patients who have had valve replacement (see Table 4: Endocarditis: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures*).
Anticoagulants are used to prevent thromboemboli (see Pulmonary Embolism: Prevention) in patients with AF.
Last full review/revision November 2012 by Guy P. Armstrong
Content last modified December 2012